| Project/Area Number |
11671515
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Anesthesiology/Resuscitation studies
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| Research Institution | Kanazawa Medical University |
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Principal Investigator |
TSUCHIDA Hideaki Kanazawa Medical University, Department of Anesthesiology, Professor, 医学部, 教授 (20155394)
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| Project Period (FY) |
1999 – 2001
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| Project Status |
Completed (Fiscal Year 2001)
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| Budget Amount *help |
¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 2001: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 2000: ¥900,000 (Direct Cost: ¥900,000)
Fiscal Year 1999: ¥1,900,000 (Direct Cost: ¥1,900,000)
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| Keywords | rat / aorta / sepsis / endothelium-dependent vasorelaxation / β-adrenergic receptor / muscarinic receptor / Ca concentration / halothane / 内皮依存性拡張 / 細胞内カルシウム濃度 / 内皮依存性血管拡張 / 細胞内Ca濃度 |
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| Research Abstract |
The mechanism (s) underlying the inhibitory effect of anesthetics or sepsis on endothelium-dependent vasorelaxation is still controversial. This study intended to clarify how anesthetics or sepsis interfered with endothelium-mediated vasorelaxation.
The volatile anesthetic halothane inhibited carbachol-induced increase in cytosolic Ca^<2+> concentration and resultant decrease in muscle tension in aconcentration-dependent manner. In addition,halothane concentration dependently inhibited nitroglycerin-induced vasorelaxation partly in a Ca^<2+>-dependent fashion. These findings strongly indicated that halothane interfered with endothelium-mediated vasorelaxation both at the NO synthetic process and at the NO-mediated vasorelaxing process. Dobutamine, a β1 adrenergic agonist, and salbutamol, a β2 adrenergic agonist, induced vasorelaxation in endothelium-intact vascular strip. In contrast, dobutamine's effect was almost abolished in endothelium-denuded strip, suggesting that dobutamine's effect was mediated by endothelium. Not only α-adrenergic receptor-mediated vasoconstriction, but β-adrenergic receptor-mediated vasorelaxation was inhibited in the septic rat aorta. Therefore, sepsis induces multifactorial inhibition on vascular relaxation.
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